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Alison K. Death

Researcher at University of Sydney

Publications -  18
Citations -  2217

Alison K. Death is an academic researcher from University of Sydney. The author has contributed to research in topics: Androgen & Androgen receptor. The author has an hindex of 16, co-authored 18 publications receiving 2122 citations. Previous affiliations of Alison K. Death include The Heart Research Institute & Royal Prince Alfred Hospital.

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Androgens and cardiovascular disease.

TL;DR: The commonality of risk factor patterns and mechanisms suggests that the efficacy of antiatherogenic therapy is an important challenge with the potential to enhance men's motivation for prevention and treatment of cardiovascular diseases.
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High glucose alters matrix metalloproteinase expression in two key vascular cells: potential impact on atherosclerosis in diabetes.

TL;DR: Evidence is provided that elevated glucose induces discordant matrix metalloproteinase (MMP) expression from two key vascular cells, endothelial cells and macrophages, which could promote matrix degradation thereby accelerating atherogenesis and potentially reducing plaque stability in diabetes.
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Androgen receptor expression is greater in macrophages from male than from female donors : A sex difference with implications for atherogenesis

TL;DR: Sex differences in androgen-mediated macrophage lipid loading may contribute to the greater prevalence and severity of atherosclerosis in men.
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The relationship between external glucose concentration and cAMP levels inside Escherichia coli: implications for models of phosphotransferase-mediated regulation of adenylate cyclase.

TL;DR: There was no striking shift in growth rate or [14C] glucose assimilation in bacteria passing through the 0.3 mM concentration threshold influencing cAMP levels, suggesting that neither metabolic flux nor transporter saturation influenced the sensing of nutrient levels.
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Dihydrotestosterone Promotes Vascular Cell Adhesion Molecule-1 Expression in Male Human Endothelial Cells via a Nuclear Factor-κB-Dependent Pathway

TL;DR: A novel AR/NF-kappaB mediated mechanism for VCAM-1 expression and monocyte adhesion operating in male endothelial cells that may represent an important unrecognized mechanism for the male predisposition to atherosclerosis is highlighted.